Ten Putative Contributors to the Obesity Epidemic

Abstract

The obesity epidemic is a global issue and shows no signs of abating, while the cause of this epidemic remains unclear. Marketing practices of energy-dense foods and institutionally-driven declines in physical activity are the alleged perpetrators for the epidemic, despite a lack of solid evidence to demonstrate their causal role. While both may contribute to obesity, we call attention to their unquestioned dominance in program funding and public efforts to reduce obesity, and propose several alternative putative contributors that would benefit from equal consideration and attention. Evidence for microorganisms, epigenetics, increasing maternal age, greater fecundity among people with higher adiposity, assortative mating, sleep debt, endocrine disruptors, pharmaceutical iatrogenesis, reduction in variability of ambient temperatures, and intrauterine and intergenerational effects as contributing factors to the obesity epidemic are reviewed herein. While the evidence is strong for some contributors such as pharmaceutical-induced weight gain, it is still emerging for other reviewed factors. Considering the role of such putative etiological factors of obesity may lead to comprehensive, cause specific, and effective strategies for prevention and treatment of this global epidemic.

Keywords:

• Obesity
• genetics
• pharmaceutical
• intrauterine
• infections

ACKNOWLEDGEMENT

Supported in part by NIH Grant P30DK056336 to DBA and NIH1R01DK066164 awarded to NVD.

Author Contribution: David Allison conceived and oversaw the project, drafted the introduction and discussion, and edited all sections. Emily McAllister, Nikhil Dhurandhar, and Scott Keith contributed to specific sections, edited the entire document, and contributed to the overall development of the manuscript. All other authors had the opportunity to edit the complete manuscript and wrote first drafts of specific sections as follows: Eisenmann contributed to the introduction; Boggiano, Hanlon and Benca to Sleep Debt; Elobeid and Ruden to Endocrine Disruptors; Pietrobelli and Barger to Ambient Temperature; Dhurandhar and McAllister to Infections; Aronne and Wright to Pharmaceutical Iatrogenesis; Baskin and Biggio to Increasing Gravida Age; Gluckman to Intrauterine and Intergenerational Effects; Waterland to Epigenetic Effects; Keith, Wang, and Fontaine to Increased Fecundity; and Redden and Katzmarzyk to Assortative mating.

Notes

¹Proposition (B) is actually something of an oversimplfication and special case of the true condition that must be met. The true and more general condition which is an easier standard to meet can be stated in terms of BMI and offspring distributions:

where τ is the BMI cutoff used to demarcate obesity (i.e., 30), g denotes a particular generation, V denotes the number of offspring, and BMI_V and BMI_U denote the BMI of an offspring and a parent, respectively.

^a Some of the observations entering into the calculations are not independent (i.e., they may be from the same subjects measured at multiple points in time). This was not taken into account in calculation of the standard errors. The Ns shown are total number of means and number of independent cohorts the means came from. The number of means will always be greater than or equal to the number of independent means, because some cohorts may have been measured at multiple points in time. However, the number of independent means can exceed the number of trials, because some trials contained more than one independent cohort. For example, six trials provided data on ziprasidone, but because the data for men and women were provided separately and several different dose conditions were used with multiple groups, the six trials yield 22 independent cohorts.

^b Estimated from the fixed effects fitted regression (see text).